Emergency oxygen therapy for the COPD patient

Emerg Med J 2001;18:333–339 333 Emergency oxygen therapy for the COPD patient R Murphy, P Driscoll, R O’Driscoll Confusion and controversy continue...
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Emerg Med J 2001;18:333–339

333

Emergency oxygen therapy for the COPD patient R Murphy, P Driscoll, R O’Driscoll

Confusion and controversy continues over how much oxygen to give patients with chronic obstructive pulmonary disease (COPD) presenting with breathlessness. This article reviews the published literature dealing with this topic, identifies gaps in the debate that have not been addressed and makes recommendations for future research needed to resolve this issue. Based on this review guidelines for oxygen therapy, based on the best evidence currently available, are then constructed and presented in a subsequent issue. Literature review METHODS

Medline from 1966 to 2000 was searched for articles on oxygen therapy and carbon dioxide retention. In addition, colleagues in chest medicine, emergency medicine and intensive care medicine identified reports presented at recent scientific research meetings. As much of the literature on oxygen therapy in COPD was published before 1966, all references made in the literature obtained were examined. Any reports subsequently felt to be relevant, were then also obtained and analysed until it was felt that a complete search had been made. REVIEW

It is useful to consider the published literature in the light of a series of clinically relevant questions:

Department of Emergency Medicine, Manchester Royal Infirmary, Oxford Road, Manchester, M13 9WL, UK R Murphy Department of Emergency Medicine, Hope Hospital, Salford, UK P Driscoll. Department of Chest Medicine, Hope Hospital R O’Driscoll Correspondence to: Dr Murphy ([email protected]) Accepted for publication 11 June 2001

What are the perceived dangers of hypoxia and at what PaO2 does it become dangerous? Significant hypoxia for more than four to six minutes will cause sudden cardiorespiratory arrest and irreversible damage to the brain and other vital organs. However, it is not known how much hypoxia is required to cause this. In 1908, Boycott and Haldane showed that a PaO2 below 45 mm Hg resulted in mental diYculties and memory loss.1 Later it was found that consciousness was lost at a PaO2 of about 30 mm Hg.2 3 Hutchison et al, in 1964, commented on this but also noted that acclimatisation to hypoxia is possible, most notably in patients with COPD.4 Subsequent studies supported this finding and recorded very low PaO2 levels when these patients have acute exacerbations (tables 1, 2 and 3). In addition, in a study in 1965, of 81 patients with acute exacerbations of chronic respiratory disease and respiratory failure, it

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Table 1

PaO2 on air in COPD patients when stable

Author

Patients (n)

Mithoefer et al, 19675 7 10 Rudolf et al, 19796 SchiV et al, 19677 9 8 Bone et al, 1978 10 Bone et al, 19788 10

Mean PaO2 (mm Hg)

Range (mm Hg)

44 49 52 75 60

38–52 39.5–58.4 29–73 49–104 42–90

Table 2 PaO2 on air in COPD patients with acute exacerbations and respiratory failure Author

Patients (n)

Mean PaO2 (mm Hg)

Range (mm Hg)

King et al, 19739 Warrell et al, 197010 Rudolf et al, 197711

40 7 3

40.4 29.8 33.6

24–68 25–28 31–39

Table 3 PaO2 on air in COPD patients when stable and when having acute exacerbations with respiratory failure

Author

Stable: range/ mean (SD) Patients (n) (mm Hg)

Hutchison et al, 19644 9 Bone et al, 19788 37 Bone et al, 19788 13 Agusti et al, 199912 18

59–74 54 (8) 55 (12) 61.5 (9.1)

Acute: range/ mean (SD) (mm Hg) 23–56 41 (9) 32 (5) 47.7 (8.7)

was found that 61 of them had PaO2 values between 20 and 40 mm Hg and two had values less than 20 mm Hg.13 In a more recent study in 2000, 13 of 15 patients with COPD developed a PaO2 less than 50 mm Hg when they undertook light exercise in simulated aircraft cabin conditions.14 All of these had a PaO2 above 70 mm Hg when breathing air at sea level. The mean oxygen saturation was 80% during this exercise but all the subjects were asymptomatic. As cardiac and respiratory emergencies are rare during commercial airline flight it is likely that, annually, many COPD patients are exposed to significant hypoxia for up to 12 hours at a time without suVering ill eVects. Consequently, some authors recommend diVerent “safe” levels of hypoxia.13 15 16 McNichol et al, suggested that a PaO2 of about 20 mm Hg is the lower limit of hypoxaemia compatible with survival, even in COPD patients.13 Hutchison et al, in 1964, suggested that a PaO2 of 50 mm Hg would prevent immediate death from hypoxia and that oxygen therapy should provide a PaO2 of at least this level.4 Later studies have supported this.17 18

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Key points x The most dangerous eVects of hypoxia are sudden cardiorespiratory arrest and irreversible damage to the vital organs. These eVects can occur within minutes. x The exact level of PaO2 that is dangerous is unclear but most patients are adequately oxygenated if the PaO2 is above 50 mm Hg. x Patients with COPD often have marked hypoxia even when stable and can tolerate this. x Patients with COPD develop further decreases in PaO2 with acute exacerbations of their condition. This can be to extremely low levels in some cases. x Many authors now recommend administering enough oxygen to keep the PaO2 above 50 mm Hg in these situations.

How much oxygen is required to relieve hypoxia? In 1960 Campbell predicted the change in arterial oxygenation that would be produced in four patients with hypercapnic respiratory failure by any given oxygen enrichment of the inspired air.19 He then went on to measure the actual increase in arterial oxygenation when these patients were given oxygen concentrations in the range 24% to 35%. He found that although the increases were, on the whole, less than predicted the diVerences were not great.20 Although no exact figures were given it was concluded that these patients were very sensitive to small changes in the concentration of inspired oxygen and that even a concentration of about 25% was certain to produce considerable relief from hypoxia. Campbell reiterated this in 1967 making reference to the oxygen dissociation curve where small changes of PaO2 in the range 25 to 40 mm Hg produce large changes in oxygen saturation.16 Other authors attempted to quantify this eVect. Hutchison et al found concentrations ranging between 24.4% and 36.4% failed to consistently produce a PaO2 over 50 mm Hg in 6 of 10 cases of acute hypercapnic respiratory failure.4 They also plotted the change in oxygen tension against the inspired oxygen concentration and saw a variation in response from patient to patient. Mithoefer et al, in 1967, studied the response of three diVerent groups of patients to 24%, 28% and 35% oxygen.5 The first was a group of normal patients. The second and third groups were patients with COPD and hypercapnic respiratory failure who were stable and hospitalised respectively. The average level of alveolar oxygen tension produced by each mask in the second group was only about 40% of that found in the first group. In the hospitalised group the arterial oxygen tension was below 50 mm Hg in 70% of patients using the 24% mask, in 35% of those using the 28% mask and in 24% of those using the 35% mask. King et al, in 1973, gave 24% oxygen to another group of patients with acute exacerbations of chronic respiratory failure.9 They recorded a mean PaO2 of 40.4 mm Hg in these

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patients on room air and a mean PaO2 of 57.3 mm Hg after 30 to 60 minutes of 24% oxygen. However, there was a marked variation in the response to oxygen and 15 of 40 patients did not increase their PaO2 beyond 50 mm Hg. Similar results have been obtained by others.7 10 In 1999 Agusti et al, gave oxygen to 18 patients with COPD, within 48 hours of an admission with acute respiratory failure.12 Oxygen was given via nasal prongs at 2–4 l/min and Venturi masks at 24%–28% in a prospective randomised crossover study. These concentrations raised the oxygen saturation to greater than 90% immediately in all cases. Oxygen was administered for 24 hours via each device and the oxygen saturation monitored continuously. Patients subsequently had an oxygen saturation less than 90% for a mean of 3.7 hours using the Venturi mask and 5.4 hours using nasal prongs. In extreme cases patients were poorly oxygenated for as long as 15 hours. It was found that the oxygen saturation was between 70% and 80% for a mean of 80 minutes, between 60% and 70% for a mean of 38 minutes and between 50% and 60% for a mean of four minutes during these periods of poor oxygenation. Again inter-subject variability was considerable. Key points x Patients with an acute exacerbation of COPD respond less well to oxygen therapy than normal patients. x The response to oxygen is variable. x A number of these patients will not increase their PaO2 beyond 50 mm Hg on low concentration oxygen.

What are the perceived dangers of carbon dioxide retention and at what PaCO2 does it become dangerous? The clinical eVects of hypercapnia have been known for some time and include depression of neurological and cardiorespiratory function.21–25 In 1955, Westlake et al described a number of cases where hypercapnia developed in COPD patients after oxygen therapy.26 One patient lapsed into a coma and fitted. Oxygen therapy was continued for six days and despite stupor, coma and muscular twitching, all related to carbon dioxide retention, the patient survived with no evidence of permanent mental impairment. A second patient developed a rise in PaCO2, headache, semi-coma and mental confusion three hours after starting oxygen therapy. This persisted for 24 hours as oxygen therapy was continued and the PaCO2 increased further. Again, the patient recovered as a compensatory metabolic alkalosis developed. A third patient had a pH of 7.26 and a PaCO2 of 72 mm Hg on admission with a rise in PaCO2 to 105 mm Hg and a fall in pH to 7.13 after four hours of oxygen therapy. This was associated with semi-coma and muscular twitching but oxygen therapy was continued. The next day the pH was 7.26 and the PaCO2 was 93 mm Hg, corresponding with a clinical improvement.

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Emergency oxygen therapy for the COPD patient

Later during his admission, he relapsed and died after developing a rise in arterial PaCO2 to 121 mm Hg and a decrease in pH to 7.12. A fourth patient developed a PaCO2 of 110 mm Hg and a pH of 7.16 after 35 hours of oxygen therapy. He slowly sank into a coma and also died. A fifth case was admitted with a pH of 7.33 and a PaCO2 of 66 mm Hg. Coma, hypoventilation and cardiac failure developed three hours after starting oxygen therapy corresponding with a pH of 7.07 and a PaCO2 of 102 mm Hg. Oxygen therapy was temporarily discontinued and then resumed. Three hours later he had recovered.

Key points x The most dangerous eVects of carbon dioxide retention are depression of neurological and cardiorespiratory function. x These eVects do not occur as quickly as those of hypoxia. x These eVects may last for a period ranging from hours to days and can resolve completely. x In some cases, however, progressive respiratory failure, a rising PaCO2 and a falling pH are eventually fatal.

As the PaCO2 and pH are interrelated, it can be diYcult to attribute the above eVects specifically to one or the other and establish at what levels of PaCO2 or pH these changes occur. A number of studies on patients with an acute exacerbation of COPD have shown survival in all patients with a pH over 7.25 and in some with a pH well below this.4 25–27 In a study published in 2000 Plant et el found that a pH less than 7.3 was associated with an increased risk of ICU admission.28 This suggests that the pH is a much more important indicator of severity and prognosis than the PaCO2. Hutchison et al, felt that in any stable patient with chronic respiratory failure, it could be assumed that the pH would be above 7.35 and that the rise in PaCO2 because of an acute exacerbation would be reflected in a fall in pH below 7.35.4 Others felt that this was why the symptoms of carbon dioxide narcosis often appear within the first 24 hours of oxygen therapy and then gradually resolve because of renal compensation. However, they also noted cases where the PaCO2 increased so slowly that the pH was relatively undisturbed permitting adaptation to hypercapnia.26 Nevertheless, they felt there was a limit to the changes in PaCO2 and pH that could occur without symptoms developing (table 4). Between these values, the mental state deteriorates as the pH falls and the PaCO2 increases. Table 4

Association between the PaCO2, the pH and clinical eVects

Authors 26

Westlake et al, 1955 Sieker et al, 195625

Mental clarity

Semi-coma or coma

pH >7.3, PCO2 7.25, PCO2